Asian Journal of Research in Dermatological Science

Premature hair greying, or premature canities, is a visible, inexpensive and easily recorded phenotype that has repeatedly been proposed as an externally observable index of accelerated biological ageing. Interest in the trait extends beyond cosmetic dermatology because loss of hair follicle pigmentation depends on the same processes that govern tissue maintenance elsewhere in the body, including somatic stem cell renewal, redox homeostasis, canonical WNT signalling, neuroendocrine regulation and cellular senescence. Several of these processes are also central to the acquisition and maintenance of bone mass, which has motivated the proposal that early greying marks individuals at elevated risk of osteopenia and fragility fracture, and additionally of thyroid disease, metabolic syndrome, dyslipidaemia and premature atherosclerosis. This review evaluates the strength, consistency and interpretability of that proposal. Priority was given to mechanistic work in human hair follicles and murine models, to observational studies relating greying to skeletal and cardiometabolic outcomes, and to genetic and syndromic evidence. The mechanistic case for shared biology is substantial: melanocyte stem cell depletion, oxidative and genotoxic injury, niche failure through basement membrane collagen loss and sympathetic hyperactivation each have close counterparts in skeletal ageing. The clinical case is considerably weaker. The skeletal literature rests on a small number of modestly sized studies with discordant results, heterogeneous case definitions, differing densitometric technologies and limited adjustment for shared confounders. Endocrine and metabolic associations are more reproducible in direction than in magnitude, and effect sizes are generally small relative to the prevalence of the trait. Genetic evidence identifies pigmentation loci rather than shared skeletal loci, and progeroid syndromes demonstrate co-occurrence under conditions of severe genomic instability that cannot be extrapolated to common variation. No prospective cohort has tested whether greying predicts incident fracture. Premature greying is therefore best regarded as a biologically informative phenotype whose diagnostic value remains unestablished, and the evidence does not currently support its use to direct skeletal or metabolic investigation.